Ask about this productRelated genes to: MYD88 antibody
- Gene:
- MYD88 NIH gene
- Name:
- MYD88 innate immune signal transduction adaptor
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 3p22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-12-23
- Date modifiied:
- 2019-04-23
Related products to: MYD88 antibody
Related articles to: MYD88 antibody
- , the spirochetal agent of Lyme disease, has a large array of lipoproteins that play a significant role in mediating host-pathogen interactions within ticks and vertebrates. While prior work has established that borrelial lipoproteins (LP) modulate immune signaling pathways, the broader transcriptional and proteomic programs induced by these molecules in macrophages are unclear. Here, we used integrated multi-omics approaches to characterize host signaling pathways activated specifically by purified borrelial lipoproteins in murine bone marrow derived macrophages (BMDMs). Single-cell RNA-Seq (scRNA-Seq) performed on BMDMs treated with various concentrations of borrelial lipoproteins revealed macrophage subsets within the BMDMs. Differential expression analysis showed that genes encoding various receptors, type I IFN-stimulated genes, signaling chemokines are upregulated while mitochondrial and ribosomal genes are downregulated in BMDMs in response to lipoproteins. Unbiased proteomics analysis of lysates of BMDMs treated with lipoproteins corroborated several of these findings. Notably, dual specificity phosphatase 1 () gene was upregulated during the early stages of BMDM exposure to LP. Pharmacological inhibition with benzylidene-3-cyclohexylamino-1-indanone hydrochloride (BCI), an inhibitor of both DUSP1 and 6 prior to exposure to LP, demonstrated that DUSP1 negatively regulates NLRP3-mediated pro-inflammatory signaling and positively regulates the expression of interferon-stimulated genes and those encoding , , and . Using human monocytic reporter cell lines, we showed MyD88- and IKK-dependent pathways contribute to mitochondrial alterations upon stimulation with lipoproteins. Extracellular flux analysis using the Seahorse assay revealed decreased oxygen consumption rate (OCR) and increased extracellular acidification rate (ECAR), indicating time-dependent metabolic reprogramming and a shift toward a glycolytic, pro-inflammatory metabolic state in BMDMs following LP stimulation. Collectively, these findings define signaling networks, regulatory nodes and metabolic alterations induced by borrelial lipoproteins in macrophages and highlight DUSP1 as a key modulator of lipoprotein-driven innate immune responses. This work provides a mechanistic framework for understanding how borrelial lipoproteins shape macrophage signaling, independent of the broader complexity of infection with intact pathogen. - Source: PubMed
Publication date: 2026/04/07
Kumaresan VenkateshPahari SusantaHung Chiung-YuHermann Brian PSchlesinger Larry SSeshu J - Garlic yellow are cultivated from bulbs under dark conditions, with cloves as natural seeds. This study explored the structural properties of differences between pre-germination garlic polysaccharides (GP) and post-germination garlic sprout polysaccharides (GSP) from garlic yellow and evaluated their effects on DSS-induced colitis mice. The results indicate germination induced glycosidic bond cleavage in GP, generating shorter chains and low-molecular-weight GSP with altered crystallinity and solubility. Both GP and GSP alleviated colitis by protecting the gut barrier, inhibiting the TLR4/MyD88/NF-κB pathway, and modulating inflammatory factors. Notably, GSP effectively elevated IL-10 levels and modulated the gut microbiota by reducing Escherichia-Shigella and increasing Akkermansia, demonstrating an advantage in anti-inflammatory mechanism compared with GP. Overall, we first evaluated the effects of germination on the functional properties of polysaccharides in garlic yellow seeds. Moreover, seeds remaining after garlic yellow mature, though considered waste products, seed-derived polysaccharide is effective in relieving colitis and shows promising applications. - Source: PubMed
Publication date: 2026/04/20
Li PeihuaGao XueMu YanquanGao HuajingQu QinglinLiu JiaqiYang FanLi DapengTan Xintong - The immunotoxicity of microplastic pollution in aquatic species is an issue of growing concern. However, the time course and mechanistic crosstalk underlying microplastic-induced hepatic injury remain poorly defined. This study examined the temporal hepatic response of Nile tilapia (Oreochromis niloticus) to 100 nm polystyrene microplastics (PS) over a 21-day exposure period, covering acute (7 days) and sub-chronic (14 and 21 days) phases. Histopathological evaluation showed no obvious liver lesions in exposed fish relative to controls at 7 days post-exposure (dpe). In contrast, progressive tissue damage marked by enhanced inflammatory cell infiltration was apparent at 14 and 21 dpe. PS exposure triggered time-dependent oxidative stress, with reactive oxygen species (ROS) and malondialdehyde (MDA) levels significantly increased and superoxide dismutase (SOD) activity decreased at 14 and 21 dpe. Ultrastructural analysis using transmission electron microscopy (TEM) further revealed distinct mitochondrial swelling and a notable increase in autophagosome numbers within hepatocytes at 7 and 14 dpe. Transcriptomic profiling indicated a biphasic dysregulation affecting both autophagy and inflammatory pathways. Specifically, autophagy-related pathways were significantly upregulated by 7 dpe, which preceded the marked activation of innate immune signaling pathways, such as NOD-like receptors (NLR) and mitogen-activated protein kinase (MAPK) signaling, observed at 14 dpe. After prolonged exposure to 21 dpe, both autophagic and inflammatory pathways were downregulated. qPCR confirmed this time-dependent expression profile for key genes associated with autophagy (sqstm1, map1lc3b, atg4d, atg5, becn1) and immune (il1β, nlrp3, tgfβ, map3k7, tnfa, tnfb, myd88) function. Pharmacological inhibition of autophagy by 3-methyladenine (3-MA) markedly abrogated the activation of NLR and MAPK signaling genes at 14 dpe, confirming a causal regulatory link between autophagy and innate immunity. Collectively, these findings suggest that microplastic exposure triggers a sequential immunotoxic transition in the fish liver. The early induction of autophagy may support subsequent immune activation, which eventually shifts to a broad suppression of immune pathways under sustained stress. This study offers new insight into the dynamic interaction between autophagy and innate immunity during microplastic-induced hepatotoxicity and highlights the potential risk of immunosuppression after long-term microplastic exposure. - Source: PubMed
Publication date: 2026/04/16
Wang FeilongGuo XiaomengGuo NaFan XiaolongXu HaiyanLi YuanyuanGao TianChen YixinZhao ChangleSun LinaWang DeshouXie XinWu Fengrui - To observe the effect of electroacupuncture (EA) on the regulation of microglia polarization in anterior cingulate cortex (ACC) by α7 nicotinic acetylcholine receptor (α7nAChR)-Toll-like receptor 4(TLR4)/nuclear factor kappa B(NF- κB) signaling pathway in chronic inflammatory pain-depression comorbidity (CIPDC) rats, so as to explore its central "analgesic-antidepressant" mechanism underlying improvement of CIPDC. - Source: PubMed
Wang TianYang PuZhang XiXu HuiHuang Wen-JingLi XinHuang Xin-YuZheng Guang-MeiXu Zhi-YiYin Li-LiHuang YingSu Sheng-Yong - Cerebral ischemia-reperfusion injury (CIRI) is a major contributor to neuronal damage after ischemic stroke, and current therapies remain limited by a narrow therapeutic window and reperfusion-associated injury. Amygdalin (Amg) has anti-inflammatory and antioxidant activities, but its role in regulating microglial polarization, pyroptosis, and the TLR4/NF-κB/NLRP3 axis in CIRI remains unclear. In this study, rat MCAO/R and BV-2 cell OGD/R models were used to evaluate the protective effects of Amg in vivo and in vitro. Transcriptomics, untargeted metabolomics, integrated pathway analysis, and molecular docking were combined with qPCR, Western blotting, LPS/ATP stimulation, and inhibitor interventions using TAK-242 and MCC950. Amg enhanced BV-2 cell viability, reduced OGD/R-induced pro-inflammatory cytokine release, and restored antioxidant enzyme activities. In MCAO/R rats, Amg significantly improved neurological function and alleviated brain tissue damage. In addition, Amg attenuated inflammation and oxidative stress, suppressed microglial M1 polarization while promoting M2-related phenotypes, and reduced pyroptosis-related marker expression in vivo and in vitro. Integrated multi-omics analysis further narrowed the candidate mechanisms to core pathways including NF-κB, Toll-like receptor, and NOD-like receptor signaling, and identified Tlr4, Myd88, Nlrp3, and Caspase-1 as key candidate molecules; pharmacological dissection experiments showed that combined treatment with Amg and either a TLR4 inhibitor or an NLRP3 inhibitor did not produce a significant additional synergistic effect, suggesting that its protective action depends on regulation of the TLR4/NF-κB/NLRP3-signaling axis. These findings provide mechanistic evidence for the neuroprotective effects of Amg in CIRI and support its potential as a therapeutic candidate for ischemic stroke. - Source: PubMed
Publication date: 2026/04/19
Wang Yan-ChenWang Hong-YanYuan Yi-FanZhang Zi-JianWang Yi-HanLiu Jing-JiePeng LiangZhang GangGao JingYan Yong-Gang